Inflammatory bowel disease (IBD), a chronic inflammatory disorder of the gastrointestinal tract suffered by approximately one million patients in the United States, is made up of two major disease groups: ulcerative colitis (UC) and Crohn's Disease (CD). In both forms of IBD, intestinal microbes may initiate the disease in genetically susceptible individuals. UC is often restricted to the colon, while CD typically occurs in the ileum of the small intestine and in the colon. (Podolsky, D. K., N. Engl. J. Med. 347:417-429 (2002). Gene expression profiling of tissue from IBD patients has provided some insight into possible targets for therapy and/or diagnosis (see, for example, Dieckgraefe, B. K. et al., Physiol. Genomics 4:1-11 (2000); Lawrance I. C. et al., Hum Mol. Genet. 10:445-456 (2001); Dooley T. P. et al., Inflamm. Bowel Dis. 10:1-14 (2004); and Uthoff S. M., Int J Oncol. 19:803-810 (2001)). Further investigations of gene dysregulation in patients experiencing inflammatory bowel disease include, or example, Lawrance, I. C. et al., who disclosed distinctive gene expression profiles for several genes in UC and CD (Lawrance, I. C. et al., Human Mol. Genetics 10(5):445-456 (2001)). Uthoff, S. M. S. et al. disclosed the identification of candidate genes for UC and CD using micro array analysis (Uthoff, S. M. S. et al., Int'l. J. Oncology 19:803-810 (2001). Dooley, T. P. et al. disclosed correlation of gene expression in IBD with drug treatment for the disorder (Dooley, T. P. et al., Inflamm. Bowel Dis. 10(1):1-14 (2004).
There is a need for the identification of additional biological markers of inflammatory bowel disease for use in diagnosis of this chronic disease. The present disclosure fills that need.
The entire contents of all references cited herein are hereby incorporated by reference.